期刊
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
卷 48, 期 5, 页码 851-858出版社
ELSEVIER SCI LTD
DOI: 10.1016/j.yjmcc.2009.12.017
关键词
Frank-Starling Law of The Heart; Length-Tension Relationship; Sarcomere length; Regulation
资金
- NIH [PO1-HL62426, RO1-HL75494, T32-007692]
- American Heart Association
- U.S. Department of Energy, Basic Energy Sciences, Office of Energy Research [W-31-109-ENG-38]
- U.S. National Institutes of Health [RR08630]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P41RR008630] Funding Source: NIH RePORTER
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL075494, T32HL007692, P01HL062426] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [P41GM103622] Funding Source: NIH RePORTER
The Frank-Starling law of the heart describes the interrelationship between end-diastolic volume and cardiac ejection volume, a regulatory system that operates on a beat-to-beat basis. The main cellular mechanism that underlies this phenomenon is an increase in the responsiveness of cardiac myofilaments to activating Ca2+ ions at a longer sarcomere length, commonly referred to as myofilament length-dependent activation. This review focuses on what molecular mechanisms may underlie myofilament length dependency. Specifically, the roles of inter-filament spacing, thick and thin filament based regulation, as well as sarcomeric regulatory proteins are discussed. Although the Frank-Starling law of the heart constitutes a fundamental cardiac property that has been appreciated for well over a century, it is still not known in muscle how the contractile apparatus transduces the information concerning sarcomere length to modulate ventricular pressure development. (C) 2009 Elsevier Ltd. All rights reserved.
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